Spatial-Explicit Climate Change Vulnerability Assessments Based on Impact Chains. Findings from a Case Study in Burundi

Climate change vulnerability assessments are an essential instrument to identify regions most vulnerable to adverse impacts of climate change and to determine appropriate adaptation measures. Vulnerability assessments directly support countries in developing adaptation plans and in identifying possible measures to reduce adverse consequences of changing climate conditions. Against this background, this paper describes a vulnerability assessment using an integrated and participatory approach that builds on standardized working steps of previously developed ‘Vulnerability Sourcebook’ guidelines. The backbone of this approach is impact chains as a conceptual model of cause–effect relationships as well as a structured selection of indicators according to the three main components of vulnerability, namely exposure, sensitivity and adaptive capacity. We illustrate our approach by reporting the results of a vulnerability assessment conducted in Burundi focusing on climate change impacts on water and soil resources. Our work covers two analysis scales: a national assessment with the aim to identify climate change ‘hotspot regions’ through vulnerability mapping; and a local assessment aiming at identifying local-specific drivers of vulnerability and appropriate adaptation measures. Referring to this vulnerability assessment in Burundi, we discuss the potentials and constraints of the approach. We stress the need to involve stakeholders in every step of the assessment and to communicate limitations and uncertainties of the applied methods, indicators and maps in order to increase the comprehension of the approach and the acceptance of the results by different stakeholders. The study proved the practical usability of the approach at the national level by the selection of three particularly vulnerable areas. The results at a local scale supported the identification of adaption measures through intensive engagement of local rural populations

The MHC2TA -168A>G gene polymorphism is not associated with rheumatoid arthritis in Austrian patients

An association between susceptibility to rheumatoid arthritis (RA) and a common -168A>G polymorphism in the MHC2TA gene with differential major histocompatibility complex (MHC) II molecule expression was recently reported in a Swedish population. The objective of the present study was to replicate this finding by examining the -168A>G polymorphism in an Austrian case–control study. Three hundred and sixty-two unrelated RA cases and 351 sex-matched and age-matched controls as well as 1,709 Austrian healthy individuals were genotyped. All participants were from the same ethnic background. Genotyping was performed using 5' allelic discrimination assays. The association between susceptibility to RA and the -168A>G single nucleotide polymorphism was examined by chi-square test. Comparison was made assuming a dominant effect (AG + GG genotypes versus AA genotype). In contrast to the primary report, the frequency of MHC2TA -168G allele carriers was not significantly different between patients and controls in the Austrian cohort. The homozygous MHC2TA -168 GG genotype was more frequent in matched controls than in Austrian RA patients. There was no association between the presence of RA-specific autoantibodies and the MHC2TA -168 GG genotype. In this cohort of Austrian patients, no association between the MHC2TA polymorphism and RA was found

Donor-But Not Recipient-Derived Cells Produce Collagen-1 in Chronically Rejected Cardiac Allografts

Fibrosis is a prominent feature of chronic allograft rejection, caused by an excessive production of matrix proteins, including collagen-1. Several cell types produce collagen-1, including mesenchymal fibroblasts and cells of hematopoietic origin. Here, we sought to determine whether tissue-resident donor-derived cells or allograft-infiltrating recipient-derived cells are responsible for allograft fibrosis, and whether hematopoietic cells contribute to collagen production. A fully MHC-mismatched mouse heterotopic heart transplantation model was used, with transient depletion of CD4+ T cells to prevent acute rejection. Collagen-1 was selectively knocked out in recipients or donors. In addition, collagen-1 was specifically deleted in hematopoietic cells. Tissue-resident macrophages were depleted using anti-CSF1R antibody. Allograft fibrosis and inflammation were quantified 20 days post-transplantation. Selective collagen-1 knock-out in recipients or donors showed that tissue-resident cells from donor hearts, but not infiltrating recipient-derived cells, are responsible for production of collagen-1 in allografts. Cell-type-specific knock-out experiments showed that hematopoietic tissue-resident cells in donor hearts substantially contributed to graft fibrosis. Tissue resident macrophages, however, were not responsible for collagen-production, as their deletion worsened allograft fibrosis. Donor-derived cells including those of hematopoietic origin determine allograft fibrosis, making them attractive targets for organ preconditioning to improve long-term transplantation outcomes

Severe T cell hyporeactivity in ventilated COVID-19 patients correlates with prolonged virus persistence and poor outcomes

Coronavirus disease 2019 (COVID-19) can lead to pneumonia and hyperinflammation. Here we show a sensitive method to measure polyclonal T cell activation by downstream effects on responder cells like basophils, plasmacytoid dendritic cells, monocytes and neutrophils in whole blood. We report a clear T cell hyporeactivity in hospitalized COVID-19 patients that is pronounced in ventilated patients, associated with prolonged virus persistence and reversible with clinical recovery. COVID-19-induced T cell hyporeactivity is T cell extrinsic and caused by plasma components, independent of occasional immunosuppressive medication of the patients. Monocytes respond stronger in males than females and IL-2 partially restores T cell activation. Downstream markers of T cell hyporeactivity are also visible in fresh blood samples of ventilated patients. Based on our data we developed a score to predict fatal outcomes and identify patients that may benefit from strategies to overcome T cell hyporeactivity.Coronavirus disease 2019 (COVID-19) can lead to pneumonia and hyperinflammation. Here we show a sensitive method to measure polyclonal T cell activation by downstream effects on responder cells like basophils, plasmacytoid dendritic cells, monocytes and neutrophils in whole blood. We report a clear T cell hyporeactivity in hospitalized COVID-19 patients that is pronounced in ventilated patients, associated with prolonged virus persistence and reversible with clinical recovery. COVID-19-induced T cell hyporeactivity is T cell extrinsic and caused by plasma components, independent of occasional immunosuppressive medication of the patients. Monocytes respond stronger in males than females and IL-2 partially restores T cell activation. Downstream markers of T cell hyporeactivity are also visible in fresh blood samples of ventilated patients. Based on our data we developed a score to predict fatal outcomes and identify patients that may benefit from strategies to overcome T cell hyporeactivity

Herstellung monoklonaler Antikörper gegen das menschliche Polycystin-2-Protein

In dieser Dissertation wird die Herstellung monoklonaler Antikörper gegen das menschliche Polycystin-2-Protein beschrieben. Aufbauend auf die Arbeiten von Köhler und Milstein wurden Myelomzellen (Zelllinie X63Ag8.6.5.3) mit antikörper-produzierenden Lymphozyten aus der Milz weiblicher Balb/c Mäuse fusioniert. Zur Immunisierung wurde ein Protein verwendet, das das C-Terminale Ende des Polycystin-2 und einen Histidin-Schwanz aufwies. Um sicherzustellen, dass die produzierten Antikörper ausschließlich gegen das C-Terminale Ende von Polycystin-2 gerichtet waren, wurden vergleichende Test mit anderen Proteinen durchgeführt. Nach zweimaliger Subklonierung ausgewählter Klone konnten zwei unabhängige monoklonale Antikörper von Klonen aus verschiedenen Fusionen erhalten werden, die mittels ELISA, Western Blot, Immunfluoreszenz und Immunpräzipitation positiv getestet wurden. Die monoklonalen Antikörper können verläßlich in der Immunfluoreszenz bis zu einer Verdünnung von 1:300 und im Western Blot bis zu einer Verdünnung von 1:1000 verwendet werden. Somit liegen 10 Jahre nach Herstellung des ersten polyklonalen Antikörpers gegen Polycystin-2 monoklonale Antikörper gegen das C-terminale Ende von Polycystin-2 mit einem breiten Anwendungsspektrum vor. Mit den hergestellten monoklonalen Antikörpern sollten sich neue Erkenntnisse und Aufschlüsse über die Funktion und Interaktion des C-terminalen Endes des menschlichen Polycystin-2-Protein erhalten lassen

Introduction of an MPEG-7 query language

Today the availability of digital media content is well established and widespread. Not only commercial content distribution is a big market, but also user driven digital multimedia content is produced and shared in big communities. One of the metadata standards that has been established to describe multimedia content via metadata is MPEG-7. This international standard facilitates many application domains and is probably the richest multimedia metadata set available today. However it does not yet exist a common query format that enables the user to query multimedia metadata databases. Therefore the MPEG committee decided to instantiate a call for proposal (N8220)for an MPEG-7 query format (MP7QF) framework and specified a set of requirements (N8219). This paper introduces a MP7QF query language and describes the background and requirements as well as the main architectural concepts and associated MP7QF XML schema types